Compare and contrast symptoms and circuits in depression with symptoms in circuits in mania.
Discuss the neurotransmitters implicated in mood disorders. For this discussion, place particular emphasis on the monoamine hypothesis of depression.
Depression and Mania
Depression is one factor that contributes to the global burden of diseases and affects people in several communities worldwide. It is a mental disorder with poor concentration, mood, low self-worth, decreased energy, and disturbed sleep. Also, depression can be accompanied by symptoms of anxiety. On the other hand, manic is a bipolar affective disorder accompanied by increased energy and elevated mood that leads to over-activity, decreased need for sleep, and pressure for speech (Marcus et al., 2012). Individuals experiencing Major depressive Disorders (MDD) show a different set of symptoms, including psychomotor impairment, retraction from social interaction, and loss of appetite. Mania is further characterized by racing thoughts, talkativeness, and excessive involvement in pleasurable activities. The efforts to cub these mental health problems are in rising globally.
Neurotransmitters Implicated in Mood Disorders
The monoamine neurotransmitters, including norepinephrine and dopamine, are the significant neurotransmitters for mood disorders and in the mechanisms of action of antidepressants. The inhibitory neurotransmitter GABA has been recognized to regulate anxiety and is the target of benzodiazepines that helps in treating anxiety disorders. The GABAergic inhibition is essential for maintaining the balance between neuronal inhibition and excitation and controls the oscillatory “pacemaker” in the brain region. The monoamine hypothesis of depression proposes that depletion of norepinephrine, serotonin, and dopamine in the CNS is the underlying pathophysiological basis for depression (Marathe et al., 2018). The mechanism of action of antidepressants supports this hypothesis by addressing that the agents that increase the levels of these neurotransmitters in the brain have shown to be effective in eliminating depressive symptoms. Intact monoamine systems require antidepressant agents to boost their therapeutic effect. However, Monoamine depletion does not increase depression symptoms in people who do not take medication, and it does not create a depression in healthy people who aren’t depressed.
Marathe, S. V., D’almeida, P. L., Virmani, G., Bathini, P., & Alberi, L. (2018). Effects of monoamines and antidepressants on astrocyte physiology: implications for monoamine hypothesis of depression. Journal of Experimental Neuroscience, 12, 1179069518789149. Retrieved from https://journals.sagepub.com/doi/abs/10.1177/1179069518789149
Marcus, M., Yasamy, M. T., van Ommeren, M. V., Chisholm, D., & Saxena, S. (2012). Depression: A global public health concern. Retrieved from https://www.who.int/mental_health/management/depression/who_paper_depression_wfmh_2012.pdf
Nuss, P. (2015). Anxiety disorders and GABA neurotransmission: a disturbance of modulation. Neuropsychiatric disease and treatment, 11, 165. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303399/